التفاصيل البيبلوغرافية
| العنوان: |
Aberrant expression of circular RNA DHPR facilitates tumor growth and metastasis by regulating the RASGEF1B/RAS/MAPK axis in hepatocellular carcinoma. |
| المؤلفون: |
Guo, Zeyi, Xie, Qingyu, Wu, Yanping, Mo, Haiyu, Zhang, Jiajun, He, Guolin, Li, Zhongzhe, Gan, Luxiang, Feng, Lei, Li, Ting, Wang, Yi, Fu, Yu, Cai, Lei, Li, Shao, Yu, Chao, Gao, Yi, Pan, Mingxin, Fu, Shunjun |
| المصدر: |
Cellular Oncology (2211-3428); Oct2023, Vol. 46 Issue 5, p1333-1350, 18p |
| مصطلحات موضوعية: |
CIRCULAR RNA, GENE expression, HEPATOCELLULAR carcinoma, METASTASIS, RAS oncogenes, TUMOR growth, PROPORTIONAL hazards models |
| مستخلص: |
Background: Circular RNAs (circRNAs) are noncoding RNAs. Accumulating evidence suggests that circRNAs play a critical role in human biological processes, especially tumorigenesis, and development. However, the exact mechanisms of action of circRNAs in hepatocellular carcinoma (HCC) remain unclear. Methods: Bioinformatic tools and RT-qPCR were used to identify the role of circDHPR, a circRNA derived from the dihydropteridine reductase (DHPR) locus, in HCC and para-carcinoma tissues. Kaplan–Meier analysis and the Cox proportional hazard model were used to analyze the correlation between circDHPR expression and patient prognosis. Lentiviral vectors were used to establish stable circDHPR-overexpressing cells. In vitro and in vivo studies have shown that tumor proliferation and metastasis are affected by circDHPR. Mechanistic assays, including Western blotting, immunohistochemistry, dual-luciferase reporter assays, fluorescence in situ hybridization, and RNA immunoprecipitation, have demonstrated the molecular mechanism underlying circDHPR. Results: CircDHPR was downregulated in HCC, and low circDHPR expression was associated with poor overall survival and disease-free survival rates. CircDHPR overexpression inhibits tumor growth and metastasis in vitro and in vivo. Further systematic studies revealed that circDHPR binds to miR-3194-5p, an upstream regulator of RASGEF1B. This endogenous competition suppresses the silencing effect of miR-3194-5p. We confirmed that circDHPR overexpression inhibited HCC growth and metastasis by sponging miR-3194-5p to upregulate the expression of RASGEF1B, which is regarded as a suppressor of the Ras/MAPK signaling pathway. Conclusions: Aberrant circDHPR expression leads to uncontrolled cell proliferation, tumorigenesis, and metastasis. CircDHPR may serve as a biomarker and therapeutic target for HCC. [ABSTRACT FROM AUTHOR] |
|
Copyright of Cellular Oncology (2211-3428) is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| قاعدة البيانات: |
Complementary Index |
Find this article in full text from Springer Verlag. 
Full Text Finder